کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1963602 | 1058481 | 2013 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
CB1 cannabinoid receptors promote maximal FAK catalytic activity by stimulating cooperative signaling between receptor tyrosine kinases and integrins in neuronal cells
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کلمات کلیدی
GPCRSp-cAMPSC-terminal Src kinaseThlCSKPTP1BRTKVEGFR2-arachidonoylglycerolECMCB1pKa2-AGSRCFAKSDSDTTEGFRBSA - BSACB1 cannabinoid receptor - CB1 گیرنده کانابینوئیدERK1/2 - ERK1 / 2Src family kinase - kinase family SrcMAPK - MAPKDAGL - NEC روزانهTetrahydrolipstatin - tetrahydrolipstatinbovine serum albumin - آلبومین سرم گاوIntegrin - اینتگرینRTK, Receptor tyrosine kinase - تیروزین کینازهای گیرنده ایdithiothreitol - دیتیوتریتولsodium dodecyl sulfate - سدیم دودسیل سولفاتTyrosine phosphorylation - فسفوریلاسیون تروفوزینdiacylglycerol lipase - لیپاز دی سیل گلیسرولExtracellular matrix - ماتریکس خارج سلولیprotein kinase A - پروتئین کیناز Amitogen-activated protein kinase - پروتئین کیناز فعال با mitogenFocal adhesion - چسبندگی کانونیfocal adhesion kinase - کیناز چسبندگی کانونیextracellular signal-regulated kinases 1 and 2 - کینازهای 1 و 2 تنظیم شده سیگنال خارج سلولیCB1 receptor - گیرنده CB1vascular endothelial growth factor receptor - گیرنده فاکتور رشد اندوتلیال عروقیEpidermal growth factor receptor - گیرنده فاکتور رشد اپیدرمالG protein-coupled receptor - گیرندههای جفتشونده با پروتئین جی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: CB1 cannabinoid receptors promote maximal FAK catalytic activity by stimulating cooperative signaling between receptor tyrosine kinases and integrins in neuronal cells CB1 cannabinoid receptors promote maximal FAK catalytic activity by stimulating cooperative signaling between receptor tyrosine kinases and integrins in neuronal cells](/preview/png/1963602.png)
چکیده انگلیسی
Tyrosine phosphorylation (Tyr-P) of focal adhesion kinase (FAK) regulates FAK activation. Phosphorylated FAK Tyr 397 binds Src family kinases (Src), which in turn directly phosphorylate FAK Tyr 576/577 to produce maximal FAK enzymatic activity. CB1 cannabinoid receptors (CB1) are abundantly expressed in the nervous system and influence FAK activation by presently unknown mechanisms. The current investigation determined that CB1-stimulated maximal FAK catalytic activity is mediated by Gi/o proteins in N18TG2 neuronal cells, and that G12/13 regulation of Rac1 and RhoA occurs concomitantly. Immunoblotting analyses using antibodies against FAK phospho-Tyr 397 and phospho-Tyr 576/577 demonstrated that the time-course of CB1-stimulated FAK 576/577 Tyr-P occurred in three phases: Phase I (0-2Â min) maximal Tyr-P, Phase II (5-20Â min) rapid decline in Tyr-P, and Phase III (>Â 20Â min) plateau in Tyr-P at submaximal levels. In contrast, FAK 397 Tyr-P was monophasic and significantly lower in magnitude. FAK 397 Tyr-P and Phase I FAK 576/577 Tyr-P involved protein tyrosine phosphatase (PTP1B and Shp1/Shp2)-mediated Src activation, Protein Kinase A (PKA) inhibition, and integrin activation. Phase I maximal FAK 576/577 Tyr-P also required cooperative signaling between receptor tyrosine kinases (RTKs) and integrins. The integrin antagonist RGDS peptide, Flk-1 vascular endothelial growth factor receptor (VEGFR) antagonist SU5416, and epidermal growth factor receptor (EGFR) antagonist AG 1478 blocked Phase I FAK 576/577 Tyr-P. CB1 agonists failed to stimulate FAK Tyr-P in the absence of integrin activation upon suspension in serum-free culture media. In contrast, cells grown on the integrin ligands fibronectin and laminin displayed increased FAK 576/577 Tyr-P that was augmented by CB1 agonists and blocked by the Src inhibitor PP2 and Flk-1 VEGFR antagonist SU5416. Taken together, these studies have identified a complex integrative pathway utilized by CB1 to stimulate maximal FAK 576/577 Tyr-P in neuronal cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 25, Issue 8, August 2013, Pages 1665-1677
Journal: Cellular Signalling - Volume 25, Issue 8, August 2013, Pages 1665-1677
نویسندگان
George D. Dalton, Lynda J. Peterson, Allyn C. Howlett,